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Resveratrol partially prevents oxidative stress and metabolic dysfunction in pregnant rats fed a low protein diet and their offspring
Author(s) -
Vega Claudia C,
ReyesCastro Luis A,
RodríguezGonzález Guadalupe L,
Bautista Claudia J,
VázquezMartínez Magaly,
Larrea Fernando,
ChamorroCevallos Germán A,
Nathanielsz Peter W,
Zambrano Elena
Publication year - 2016
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp271543
Subject(s) - offspring , endocrinology , oxidative stress , medicine , leptin , pregnancy , resveratrol , biology , insulin , corticosterone , fetus , hormone , obesity , biochemistry , genetics
Key points Maternal protein restriction during pregnancy increases both maternal and offspring oxidative stress and leads to metabolic dysfunction. Maternal low protein diet during pregnancy increases maternal and offspring corticosterone. Resveratrol administration partially prevents both maternal and offspring adverse outcomes induced by maternal protein restriction during pregnancy.Abstract Protein restriction in pregnancy produces maternal and offspring metabolic dysfunction potentially as a result of oxidative stress. Data are lacking on the effects of inhibition of oxidative stress. We hypothesized that maternal resveratrol administration decreases oxidative stress, preventing, at least partially, maternal low protein‐induced maternal and offspring metabolic dysfunction. In the present study, pregnant wistar rats ate control (C) (20% casein) or a protein‐restricted (R) (10% casein) isocaloric diet. Half of each group received resveratrol orally, 20 mg kg −1 day −1 , throughout pregnancy. Post‐delivery, mothers and offspring ate C. Oxidative stress biomarkers and anti‐oxidant enzymes were measured in placenta, maternal and fetal liver, and maternal serum corticosterone at 19 days of gestation (dG). Maternal (19 dG) and offspring (postnatal day 110) glucose, insulin, triglycerides, cholesterol, fat and leptin were determined. R mothers showed metabolic dysfunction, increased corticosterone and oxidative stress and reduced anti‐oxidant enzyme activity vs . C. R placental and fetal liver oxidative stress biomarkers and anti‐oxidant enzyme activity increased. R offspring showed higher male and female leptin, insulin and corticosterone, male triglycerides and female fat than C. Resveratrol decreased maternal leptin and improved maternal, fetal and placental oxidative stress markers. R induced offspring insulin and leptin increases were prevented and other R changes were offspring sex‐dependent. Resveratrol partially prevents low protein diet‐induced maternal, placental and sex‐specific offspring oxidative stress and metabolic dysfunction. Oxidative stress is one mechanism programming offspring metabolic outcomes. These studies provide mechanistic evidence to guide human pregnancy interventions when fetal nutrition is impaired by poor maternal nutrition or placental function.